title: Expression levels of CD47, CD35, CD55, and CD59 on red blood cells and signal-regulatory protein-alpha,beta on monocytes from patients with warm autoimmune hemolytic anemia.
abstract: BACKGROUND
  Animal models have shown that CD47-deficient mice develop severe autoimmune hemolytic anemia (AIHA) because the binding of red blood cell (RBC) CD47 to signal-regulatory protein (SIRP-alpha) on macrophages contributes to the inhibition of phagocytosis. In contrast, complement-inhibitory proteins such as CD35, CD55, and CD59 may protect RBCs against the lysis by complement.
  
  
  METHODS
  With the use of flow cytometric analyses, the expression of CD47, CD35, CD55, and CD59 on RBCs and of SIRP-alpha,beta on peripheral monocytes of 36 patients with warm AIHA (wAIHA; 23 with active wAIHA, 13 with wAIHA in remission) and 20 healthy subjects was evaluated.
  
  
  RESULTS
  The mean fluorescence intensities (MFIs) of the expression of CD47, CD35, CD55, and SIRP-alpha,beta of active wAIHA patients, wAIHA in remission, and healthy subjects were not statistically different. Patients with active wAIHA showed significantly lower CD59 expression on RBCs than healthy individuals (MFI, 512.5 +/- 59.6 vs. 553.7 +/- 36.6; p = 0.009), while the CD59 expression in patients with wAIHA in remission was not significantly different from that of healthy controls (MFI, 538.4 +/- 48.3 vs. 553.7 +/- 36.6; p > 0.05). The expression of CD59 on RBCs of 3 patients who died from the wAIHA was lower than that seen on RBCs of healthy controls (MFI, 433.6 +/- 69.6 vs. 553.74 +/- 36.6; p = 0.0001).
  
  
  CONCLUSIONS
  Our data show that the expression of CD47 on RBCs and SIRP-alpha,beta on monocytes of patients with wAIHA is not different from that seen in healthy individuals. In addition, we detected that patients with active wAIHA present low expression of CD59 and normal expression of CD35 and CD55 on their RBCs. Complement-regulatory proteins may play an important role in protecting RBC destruction through the activation of complement.
authors.affiliation: Faculdade de Ciências Médicas, Universidade Federal de São Paulo, Santa Casa de São Paulo, São Paulo, Brasil.
authors.forename: Melca M O
authors.initials: MM
authors.lastname: Barros
authors.forename: Mihoko
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Maria S
authors.initials: MS
authors.lastname: Figueiredo
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Cançado
authors.forename: Elisa Y S
authors.initials: EY
authors.lastname: Kimura
authors.forename: Dante M
authors.initials: DM
authors.lastname: Langhi
authors.forename: Carlos S
authors.initials: CS
authors.lastname: Chiattone
authors.forename: Jose O
authors.initials: JO
authors.lastname: Bordin
mesh_terms: D000328:Adult; D000368:Aged; D000744:Anemia, Hemolytic, Autoimmune / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis* / Q000235:genetics; D051928:CD47 Antigen / Q000096:biosynthesis* / Q000235:genetics; D018958:CD55 Antigens / Q000096:biosynthesis* / Q000235:genetics; D018957:CD59 Antigens / Q000096:biosynthesis* / Q000235:genetics; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D010587:Phagocytosis / Q000235:genetics; D017463:Receptors, Complement 3b / Q000096:biosynthesis* / Q000235:genetics; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D000943:Antigens, Differentiation; D051928:CD47 Antigen; C497894:CD47 protein, human; D018958:CD55 Antigens; D018957:CD59 Antigens; C509991:CR1 protein, human; C497895:Cd47 protein, mouse; D017463:Receptors, Complement 3b; D011971:Receptors, Immunologic; C501920:SIRPA protein, human; C051590:CD59 protein, human